Interferences with Urinary Elimination Urinary Elimination “Bones can break, muscles can atrophy, glands can loaf, even the brain can go to sleep without immediate danger to survival. But should the kidneys fail….neither bone, muscle, gland, nor brain could carry on.” Urinary System Kidneys Macrostructure Paired, reddish, brown bean-shaped organs Location: Retroperitoneal on either side of the vertebral column 12th thoracic vertebrae to 3rd Lumbar Left kidney is 1.5 to 2 cm higher than right Weight: 115 – 175 gms (4-6 ounces) Adrenal Gland lies on top of each kidney Kidneys Microstructure Nephron -- Functional unit of kidney, forms urine Each kidney has 1 million nephrons Each Nephron is composed of: Cortex: glomerulus, Bowman’s capsule, proximal convoluted tubule, distal convoluted tubule Medulla: The loop of Henle and collecting ducts Kidneys Microstructure Glomerulus – selective filtration Bowman’s Capsule – semipermeable membrane / hydrostatic pressure changes Proximal tubule: Active transport Reabsorption of 80% of electrolytes & water Reabsorption of all glucose & amino acids Reabsorption of HCO3- Acid-Base Balance Reabsorption of Creatinine Loop of Henle: Reabsorption of Na+ & Cl- in ascending limb Reabsorption of water in descending loop Concentration of filtrate Kidneys Microstructure Distal Tubule: Secretion of K+, H+, ammonia Reabsorption of water (regulated by ADH) Reabsorption of HCO3- -- Acid-Base Balance Regulation of Ca++ and PO4- by parathyroid hormone Regulation of NA+ & K+ by aldosterone Collecting Duct: Reabsorption of water (ADH required) Blood Supply Blood reaches kidney via renal artery 20-25% of cardiac output 1200 ml per minute TO KIDNEY: Aorta – renal artery – kidney hilus Renal artery divides into secondary branches, then into smaller braches to afferent arteriole Capillary network – Glomerulus FROM KIDNEY: Efferent arteriole – Peritubular capillaries – Renal vein – inferior vena cava Nephron Function Physiology of Urine Formation Normal glomerular function- Urine formation starts at glomerulus where blood is filtered GFR-(Glomerular filtration rate)- amt of blood filtered by glomeruli in a given time Normal GFR- 125ml/minute, however only 1 ml per minute becomes urine, most is reabsorbed Nephron Function Renal Function Other Kidney Functions Hormone Production Erythropoietin In response to hypoxia & decreased renal blood flow Stimulates RBC production in the bone marrow Deficiencies lead to anemia in renal failure Renin Released from juxtaglomerular apparatus of the nephron In response to < arterial BP, renal ischemia, > NA+ concentration Splits angiotensinogen into angiotensin I = angiotensin II Stimulates aldosterone from the adrenal cortex = water + NA+ retention + peripheral vasoconstriction Renin-angiotensinaldosterone System Other Kidney Functions Hormone Production Prostaglandins (PGs) Kidney medulla Vasodilating action = increases renal blood flow and promotes NA+ excretion Counteracts the vasoconstrictor effect of angiotensin and norepinephrine Lowers arterial BP by decreasing systemic vascular resistance Active metabolite of Vitamin D – second step in activating Vitamin D after action of ultraviolet radiation on cholesterol in the skin Nursing Process Alterations in Urinary Function Assessment: Patient history Physical Assessment: inspection, percussion, palpation Assessment of Urine: color, clarity, odor Urine testing & specimen collection Urinalysis, C&S, Composite urine collection Creatinine Clearance – 85-135ml/min Diagnostic tests: KUB (kidney, ureter, bladder) renal ultrasound, renal CT scan Invasive: IVP, Cystoscopy, arteriogram, urodymanics Upper Urinary Tract Infections Acute Pyelonephritis Chronic Pyelonephritis Acute Glomerulonephritis Acute Poststreptococcal Glomerulonephritis Chronic Glomerulonephritis Acute Pyelonephritis Inflammation of the renal parenchyma and collecting system Most common cause: bacterial (E.coli, Proteus, Klebsiella, Enterobacter species) Pre-existing factor: vesicoureteral reflux Commonly begins in the renal medulla and spreads to the adjacent cortex Recurring episodes may lead to chronic pyelonephritis Urosepsis: bacteriuria and bacteremia Acute Pyelonephritis Clinical Manifestations: sudden chills, fever, vomiting, malaise, flank pain, and lower UTI symptoms of cystitis Diagnostics: Urinalysis: pyruia, bacteriuia, hematuria Imaging Studies: IVP, CT Scan, Ultrasonography of the urinary system Acute Pyelonephritis Medical Management for Mild Symptoms: Short hosp stay for IV antibiotic or OP oral antibiotics Empiric broad spectrum (Ampicillin / Vancomycin) combined with aminoglycoside Change to sensitivity-guided therapy when culture results are available for 14-21 days Sulfa—Bactrim / Cipro / Floxin Adequate fluid intake Nonsteroidal antiinflammatory drugs Antipyretic drugs Urinary analgesics – Pyridium Follow-up cultures & imaging studies Relapse may occur – treated with 6-week course of antibiotics Antibiotic prophylaxis Acute Pyelonephritis Medical Management for Severe Symptoms: Hospitalization Parenteral antibiotics Broad-spectrum – switch to sensitivity specific Followed by oral antibiotics 7-21 days Adequate fluid intake – parenteral until symptoms of N/V, dehydration subside Relieve pain Treat fever Urinary antiseptics Follow-up culture imaging studies Chronic Pyelonephritis Term used to describe a kidney that has lost function due to scarring and fibrosis Result of chronic upper urinary tract infections Other names: interstitial nephritis, chronic atrophic pyelonephritis, reflux nephropathy Level of renal function depends on: whether one or both kidneys are affected magnitude of scarring the presence of co-existing infection Progresses to end-stage renal disease when both kidneys are affected Acute Glomerulonephritis Immunologic process resulting in inflammation of the glomeruli Usually affects both kidneys equally Tubular, interstitial, and vascular changes occur Etiology: Two types: Antibodies have specificity for antigens within the glomerular basement membrane (GBM) – produce autoantibodies – to one’s own tissue -- mechanism unknown Antibodies react with circulating nonglomerular antigens and are randomly deposited as immune complexes along the GBM End result: glomerular injury as a result of inflammation Acute Glomerulonephritis Clinical Manifestations: Varying degrees of hematuria Varying degrees of urinary excretion of WBC and casts Proteinuria Elevated BUN and Creatinine and Albumin + renal biopsy Medical Management: Rest Sodium and fluid restriction Diuretics Antihypertensive therapy Decreased dietary protein Glomerulonephritis Chronic Glomerulonephritis Syndrome – end-stage glomerular inflammatory disease Proteinuria, hematuria, slow development of uremic syndrome = decreased renal function Slow course toward renal failure over a few to as many as 30 years Often found coincidentally with abnormal UA or elevated blood pressure Confirmed with ultrasound and CT scan – Renal Bx Medical Management: Treat HTN Treat UTIs Protein and Phosphate restriction Acute Poststreptococcal Glomerulonephritis Most common in children & young adults 5-21 days after a streptococcal sore throat or impetigo Nephrotoxic strains of group A B-hemolytic streptococci Antibodies are produced to the strept antigen Unknown mechanism – the antigen-antibody complexes are deposited in the glomeruli – leads to = decreased glomerular filtration & inflammation Acute Poststreptococcal Glomerulonephritis Clinical Manifestation: Generalized body edema, hypertension, oliguria, hematuria, oliguria, proteinuria, fluid retention, edema in low-pressure tissues – periorbital edema abdominal or flank pain Patient may be asymptomatic – UA finding Diagnostics: Antistreptolysin O (ASO) titers Renal biopsy Erythroycte casts Elevated BUN and Creatinine Acute Poststreptococcal Glomerulonephritis Medical Management: Rest until signs of glomerular inflammation subside (proteinuria & hematuria) Treat hypertension Restrict sodium & fluid intake Antibiotics only if streptococcal infection is still present Prevention: Early diagnosis & treatment of sore throats and skin lesions; good personal hygiene, patient adherence to antibiotic therapy Renal Conditions Polycystic Kidney Renal Artery Stenosis Renal Tuberculosis HIV—associated Nephropathy Nephrotic Syndrome Polycystic Kidney One of the most common genetic diseases Two forms: Childhood manifestation: rare autosomal recessive disorder with rapid progression Adult manifestation: autosomal dominant disorder – latent – 30-40 years of age Involves both kidneys Cortex & medulla are filled with thin-walled cysts that are several mm – cm in diameter Cysts enlarge – contain blood and pus - destroy surrounding tissue Polycystic Kidney Clinical Manifestation: Symptoms appear when the cysts begin to enlarge Abdominal and/or flank pain Palpable enlarged kidneys Hematuria UTI Hypertension Diagnosis: Family History, IVP, ultrasound, CT scan Usually progresses to end-stage renal failure Renal Artery Stenosis Partial occlusion of one or both renal arteries Atherosclerotic narrowing or fibromuscular hyperplasia 1-2% of hypertension Diagnosis: Renal arteriogram Therapy Goal: Control hypertension Restore kidney perfusion Percutaneous transluminal renal angioplasty Surgical revascularization (splenic artery or aorta) Renal Artery Stenosis Renal Tuberculosis Rarely a primary lesion Onset 5-8 years after primary pulmonary TB Initially asymptomatic Low grade fever, when infection descends to bladder: polyuria, dysuria, epididymitis in men Diagnosis: TB in Urine; IVP Long Term: scarring of renal parenchyma & ureteral strictures Earlier the treatment – less likely renal failure will occur Five drugs: Isoniazid (INH), rifampin, pyrazinamide, streptomycin, ethambutol HIV—associated Nephropathy Range from mild fluid & electrolyte abnormalities to progressive renal impairment and renal failure 10% incidence – highest among IV drug users Clinical Manifestations: Proteinuria & nephrotic syndrome Progressive azotemia, enlarged kidney, rapid progression to end-stage renal failure Acute renal failure: most commonly seen in patients with AIDS who is critically ill with HIV-related infection or malignancy Treatment: Depends on treatment of primary disease - Dialysis Nephrotic Syndrome Decreased urine output Proteinuria Volume overload CHF Dysrhythmias N/V Uremic frost Anemia Vascular & Tubular Pathogenesis Nephrotic Syndrome Increase in nitrogen waste in blood Fluid and electrolyte disturbance Treatment either conservative or aggressive Renal Disease Assessment - Labs Elevated BUN Elevated creatinine Elevated potassium Elevated phosphate Decreased calcium Decreased HCO3 and pH Renal Disease Treatment Conservative Medication, diet & fluid restriction Aggressive Renal Replacement Therapies: Dialysis (Peritoneal or Hemo) Organ transplantation Acute Renal Failure 4+ Pitting Edema Renal Disease Nursing Process Assess: comprehensive pain assessment; monitor urinary output—color, frequency, consistency, volume, odor; neuro, CV—wt, edema, respiratory, skin integrity; GI-abd girth Nsg Action: Admin meds—pain relief, antibiotics, treat HTN, fluid restriction versus hydration– IV & po; hygiene; prepare for testing, procedures, surgery Pt Education: Meds; nutrition, fluid restriction, hygiene; pathology & strategies to promote adherence Peritoneal Dialysis Hemodialysis Renal Transplant Ureters Renal pelvis holds 3-5 ml of urine Kidney damage may result from backflow of more than that amount of urine – REFLUX UVJ (Ureteropelvic junction) – closes based on the ureter’s angle of bladder penetration and muscle fiber attachments to prevent backflow During coughing or voiding – muscle fibers contract to promote ureteral lumen closure The bladder then contracts to further close the UVJ and prevent urine from moving back through Nephrolithiasis 500,000 people in US annually 20-55 years of age More common in men than women Except for struvite stones associated with UTI No single theory can account for stone formation Urinary pH, solute load, urinary stasis, urinary infection with urea-splitting bacteria Five major categories: Calcium phosphate Calcium oxalate Uric acid Cystine Struvite Risk Factors for the Development of Renal Calculi Metabolic: Increased urine levels of calcium, oxaluric acid, uric acid, citric acid Climate: Warm climates cause increase fluid loss, low urine volume, and increased solute concentration in urine Diet: Proteins that increase uric acid excretion Excessive amounts of tea or fruit juices that elevate urinary oxalate level Large intake of calcium and oxalate Low fluid intake Genetic Factors: Family history of stone formation, cystinuria, gout, renal acidosis Lifestyle: Sedentary occupation, immobility Types of Renal Calculi Renal Calculi Clinical Manifestation: Abdominal or flank pain Hematuria “Renal Colic” – passing into the ureter Nausea & vomiting Chills, fever Diagnosis: UA, Urine C&S, IVP, retrograde pyelogram, ultrasound, cystoscopy Renal function: BUN, Serum Creatinine Renal Calculi Medical Management: Acute: treat pain, infection, obstruction Narcotics, for fluids—IV and po, strain urine Evaluate cause of stone formation: history, stone analysis Adequate hydration, dietary NA+ restriction, dietary changes, medication Treatment of struvite stones: control of infection Renal Calculi Removal Indications for Endourologic, lithotripsy or open surgical stone removal: Stones too large for spontaneous passage Stones associated with bacteriuria or symptomatic infection Stones causing impaired renal function Stones causing persistent pain, nausea, or ileus Inability of patient to be treated medically Patient with one kidney Renal Calculi Removal Endourological Procedures Cystoscopy – remove stones from bladder Cystolitholapaxy – cysto with lithotrite (stone crusher) – then flushed out of bladder Cystoscopic lithotripsy – cysto with pulverize stones Flexible ureteroscopes: remove stones from ureter, kidney pelvis – may be used with ultrasound, electrohydraulic, or laser lithotripsy Percutaneous nephrolithotomy -- nephrostomy tube left in place for a period of time Percutaneous Nephrostomy Renal Stents Incisions for Kidney Surgery Renal Calculi Removal Invasive Lithotripsy Percutaneous ultrasonic lithotripsy – via percutaneous nephroscope Electrohydraulic lithotripsy – percutaneous Laser lithotripsy probes – lower ureteral and large bladder stones Non-invasive - Extracorporeal shock-wave lithotripsy Patient is anesthetized High-energy acoustic shock waves shatter stone without damaging surrounding tissue Lithotripsy Renal Calculi Nursing Diagnoses Acute pain Anxiety r/t uncertain outcome Ineffective therapeutic regimen management Impaired urinary elimination Risk for infection Renal Calculi Nursing Management Assess: Pain—guarding, pain scale, occurrence— colic versus ongoing, tenderness on palpation; History: recent/chronic UTI, immobility, gout, hyperparathyroidism, prostatic hyperplasia; family history of calculi; urine output; oliguria, hematuria; labs—BUN, CR, UA, Urine C&S, Increased uric acid, calcium Action: Relieve pain; Treat UTI; Admin meds; Force fluids PO - >2L/day; Maintain IV patency; strain urine; position of comfort Pt Education: Rationale for treatment; Measures to prevent future recurrence (once calculi origin is determined)—dietary restrictions (purine, calcium, oxalates Renal Calculi Nutritional Therapy Foods high in purine, calcium, or oxalate: Purine: High: Sardines, herring, mussels, liver, kidney, goose, venison, meat soups sweetbreads Moderate: Chicken, salmon, crab, veal, mutton, bacon, pork, beef, ham Calcium: milk, cheese, ice cream, yogurt, sauces containing milk, all beans (except green beans), lentils, fish with fine bones (sardines, kippers herring, salmon); dried fruits, nuts, chocolate, cocoa, Ovaltine Oxalate: spinach, rhubarb, asparagus, cabbage, tomatoes, beets, nuts, celery, parsley, runner beans, chocolate, cocoa, instant coffee, Ovaltine, tea; Worcestershire sauce