NCLEX: Renal and urologic disorders

Chronic renal failure

Typically the result of a gradually progressive loss of renal function, chronic renal failure occasionally results from a rapidly progressive disease of sudden onset. Few signs and symptoms develop until after more than 75% of glomerular filtration is lost. Then the remaining normal parenchyma deteriorate progressively,and signs and symptoms worsen as renal function decreases. If this condition continues unchecked, uremic toxins accumulate and produce potentially fatal physiologic changes in all major organ systems.

 

What causes it
Causes of chronic renal failure include:
• chronic glomerular disease such as glomerulonephritis
• chronic infections, such as chronic pyelonephritis and tuberculosis
• congenital anomalies such as polycystic kidney disease
• vascular diseases, such as renal nephrosclerosis and hypertension
• obstructive processes such as calculi
• collagen diseases such as systemic lupus erythematosus
• nephrotoxic agents such as long-term aminoglycoside therapy
• endocrine diseases such as diabetic neuropathy
• acute renal failure that fails to respond to treatment.

Pathophysiology
Nephron damage is progressive. When nephrons are damaged, they can’t function. Healthy nephrons compensate for damaged nephrons by enlarging and increasing their clearance capacity. The kidneys can maintain relatively normal function until about 75% of the nephrons are nonfunctional.

Unbearable burden

Eventually, the healthy glomeruli are so overburdened they become sclerotic and stiff, leading to their destruction as well. If this condition continues unchecked, toxins accumulate and produce potentially fatal changes in all major organ systems.

What to look for
The degree of renal failure partly determines the frequency and severity of clinical manifestations.

What tests tell you
• Creatinine clearance tests can identify the stage of chronic renal failure. Reduced renal reserve occurs when the creatinine clearance GFR is 40 to 70 ml/minute. Renal insufficiency occurs at a GFR of 20 to 40 ml/minute, renal failure at a GFR of 10 to 20 ml/minute, and end-stage renal disease at a GFR of less than 10 ml/ minute.
• Blood studies show elevated BUN, creatinine, and potassium levels; decreased arterial pH and bicarbonate levels; and a low Hb level and HCT.
• Urine specific gravity becomes fixed at 1.010; urinalysis may show proteinuria, glycosuria, erythrocytes, leukocytes, and casts, depending on the cause.
• X-ray studies include KUB films, excretory urography, nephrotomography, renal scan, and renal arteriography.
• Kidney biopsy allows histologic identification of the underlying abnormality.

How it’s treated
The major goal of treatment early in the disease is to preserve existing kidney function and to correct specific symptoms. Conservative measures include a low-protein diet to reduce the production of end products of protein metabolism that the kidneys can’t excrete. However, a patient receiving continuous peritoneal dialysis should have a high-protein diet. The patient should also consume enough calories to prevent weight loss and catabolism.

He should restrict sodium and potassium consumption as well. Maintaining fluid balance requires careful monitoring of vital signs, weight changes, and urine output.

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Send in the drugs

Drug therapy commonly relieves associated signs and symptoms, but medications excreted by the kidneys may require dosage adjustments. Avoid using antacids or laxatives that contain magnesium to prevent magnesium toxicity. Drugs commonly used to treat chronic renal failure include:
• antipruritics, such as diphenhydramine (Benadryl) to relieve itching, and calcium carbonate to lower serum phosphate levels
• vitamin supplements (particularly B vitamins and vitamin D) and essential amino acids to relieve deficiencies caused by inadequate intake (from anorexia or dietary restrictions), altered metabolism (from uremia and medications), or increased losses of vitamins during dialysis
• loop diuretics, such as furosemide (if some renal function remains), along with fluid restriction to reduce fluid retention
• digoxin (Lanoxin) to mobilize edema fluids
• antihypertensives to control blood pressure and associated edema
• antiemetics taken before meals to relieve nausea and vomiting
• famotidine (Pepcid) or nizatidine (Axid) to decrease gastric irritation.

Anemia ailments

Anemia necessitates iron and folate supplements; severe anemia requires infusion of fresh frozen packed cells or washed packed cells. Even so, transfusions only temporarily relieve anemia. Epoetinalfa may be administered to increase RBC production. Treatment may also include cleaning enemas to remove blood from the GI tract detected through regular stool analysis (guaiac test).

Dialysis dilemmas

Hemodialysis or peritoneal dialysis — particularly such techniques as continuous ambulatory peritoneal dialysis and continuous cyclic peritoneal dialysis — can help control most manifestations of end-stage renal disease. Altering dialyzing bath fluids can correct fluid and electrolyte disturbances. However, anemia, peripheral neuropathy, cardiopulmonary and GI complications, sexual dysfunction, and skeletal defects may persist. Also, maintenance dialysis may produce complications, such as protein wasting, refractory ascites, dialysis dementia, and hepatitis B from numerous blood transfusions.

What to do
• Monitor potassium levels.
• Assess hydration status carefully. Check for jugular vein distention and auscultate the lungs for crackles. Measure daily intake and output carefully. Record daily weight and the presence or absence of thirst, axillary sweat, dry tongue, hypertension, and peripheral edema.
• Observe for signs of bleeding.
• If the patient requires dialysis, explain the procedure fully and watch for complications during and after the procedure.
• Evaluate the patient. After successful therapy, the patient verbalizes an understanding of the disease process and medical regimen, exhibits no signs of complications, and has his signs and symptoms controlled by dialysis or transplantation. He has normal BUN, creatinine, and electrolyte levels and maintains a satisfactory diet with normal bowel function.

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Lower UTIs

Lower UTIs commonly respond readily to treatment, but recurrence and resistant bacterial flare-up during therapy are possible. Lower UTIs are nearly 10 times more common in women than in men and affect 1 in 5 women at least once. Lower UTIs also occur in relatively large percentages in sexually active teenage girls.
Lower UTIs fall into two types:

  • cystitis, which is an inflammation of the bladder that usually results from an ascending infection
  • urethritis, which is an inflammation of the urethra.

What causes it
Causes of lower UTIs include:
• infection by gram-negative enteric bacteria, such as Escherichia coli, Klebsiella, Proteus, Enterobacter, Pseudomonas, or Serratia
• simultaneous infection with multiple pathogens in a patient with neurogenic bladder
• an indwelling urinary catheter
• fistula between the intestine and bladder.

Pathophysiology
Recent studies suggest that infection results from a breakdown in local defense mechanisms in the bladder that allows bacteria to invade the bladder mucosa and multiply. These bacteria can’t be readily eliminated by normal micturition.

What to look for
Characteristic signs and symptoms include:
• urinary urgency and frequency
• dysuria
• bladder cramps or spasms
• itching
• feeling of warmth during urination
• nocturia
• possibly hematuria
• fever
• urethral discharge in males.
Other common features include lower back pain, malaise, confusion, nausea, vomiting, abdominal pain or tenderness over the bladder, chills, and flank pain.

What tests tell you
• Microscopic urinalysis showing RBC and WBC levels greater than 10/high-power field points to UTI. A clean midstream urine specimen revealing a bacterial count of more than 100,000/ml confirms it. Sensitivity testing suggests the appropriate therapeutic antimicrobial agent.
• A blood test or stained smear rules out venereal disease.
• Voiding cystourethrography or excretory urography may detect congenital anomalies.

How it’s treated
A 7- to 10-day course of an appropriate antibiotic is usually the treatment of choice for initial lower UTI. After 3 days of antibiotic therapy, a urine culture should show no organisms. If the urine isn’t sterile, bacterial resistance has probably occurred, requiring a different antimicrobial. Single-dose antibiotic therapy with amoxicillin or ciprofloxacin may be effective in women with acute noncomplicated UTI. A urine culture taken 1 to 2 weeks later indicates whether the infection has been eradicated.

It’s back…

Recurrent infections caused by renal calculi, chronic prostatitis, or a structural abnormality may require surgery. If the patient has no predisposing conditions, she will most likely receive long-term, low-dose antibiotic therapy.

What to do
• Collect all urine specimens for culture and sensitivity testing carefully and promptly.
• Watch for GI disturbances from antibiotic therapy. Nitrofurantoin macrocrystals, taken with milk or a meal, prevent such distress.
• Evaluate the patient. After successful treatment, the patient can explain the relation between personal hygiene and UTIs. She can describe hygiene practices to prevent UTIs and has completed the prescribed course of antibiotic therapy.

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Nephrotic syndrome

Nephrotic syndrome (NS) is a condition characterized by marked proteinuria, hypoalbuminemia, hyperlipidemia, and edema. Although NS isn’t a disease itself, it results from a specific glomerular defect and indicates renal damage.

What causes it
• Primary (idiopathic) glomerulonephritis (affecting children and adults)
• Diabetes mellitus
• Collagen vascular disorders
• Circulatory diseases
• Nephrotoxins
• Allergic reactions
• Infection
• Pregnancy
• Hereditary nephritis
• Multiple myeloma and other neoplastic diseases

Pathophysiology
Regardless of the cause, the injured glomerular filtration membrane allows the loss of plasma proteins, especially albumin and immunoglobulin. Hypoalbuminemia results not only from urine loss but also from decreased hepatic synthesis of replacement albumin. Hypoalbuminemia stimulates the liver to synthesize lipoprotein (with consequent hyperlipidemia) and clotting factors. Decreased dietary intake (as with anorexia, malnutrition, or concomitant disease) further contributes to decreased plasma albumin levels. Loss of immunoglobulin also increases susceptibility to infection.

Runnin’ on empty

Extensive proteinuria (more than 3.5 g/day) and a low serum albumin level lead to low serum colloid osmotic pressure and edema. The low serum albumin level also leads to hypovolemia and compensatory salt and water retention. Consequent hypertension may precipitate heart failure in compromised patients.

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What to look for
The dominant clinical feature in NS is mild to severe dependent edema of the ankles or sacrum or (especially in children) periorbital edema. It may lead to ascites, pleural effusion, and swollen external genitalia. Other signs and symptoms include:
• foamy urine
• orthostatic hypotension
• lethargy
• anorexia
• depression
• pallor.

What tests tell you
• Urine testing that reveals consistent proteinuria in excess of 3.5 g/day; an increased number of hyaline, granular, and waxy, fatty casts; and oval fat bodies strongly suggests NS.
• Increased cholesterol, phospholipid, and triglyceride levels and decreased albumin levels support the diagnosis.
• Histologic identification of the lesion requires kidney biopsy.

How it’s treated
Effective treatment necessitates correction of the underlying cause if possible. Supportive treatment consists of:
• protein replacement with a nutritional diet of 1 g of protein per kilogram of body weight
• restricted sodium intake
• diuretics for edema
• antibiotics for infection.
Some patients respond to an 8-week course of corticosteroid therapy (such as prednisone), followed by a maintenance dose. Others respond better to a combination course of prednisone and azathioprine (Imuran) or cyclophosphamide (Cytoxan).

What to do
• Frequently check urine for protein. (Urine that contains protein appears frothy.)
• Measure blood pressure while the patient is supine and while he’s standing; immediately report a drop in blood pressure that exceeds 20 mm Hg.
• Monitor intake and output, and check weight at the same time each morning.
• Ask the dietitian to plan a moderate-protein, low-sodium diet.

• Provide good skin care because the patient with NS usually has edema.
• To avoid thrombophlebitis, encourage activity and exercise and provide antiembolism stockings as ordered.
• To prevent GI complications, administer steroids with an antacid or with cimetidine (Tagamet) or ranitidine (Zantac).
• Evaluate the patient. After successful therapy, the patient is prepared to follow dietary and medical regimens at home, has no proteinuria, and exhibits no signs of complications.

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Neurogenic bladder

Neurogenic bladder refers to any bladder dysfunction caused by an interruption of normal bladder innervation. Other names for this disorder include neuromuscular dysfunction of the lower urinary tract, neurologic bladder dysfunction, and neuropathic bladder.

What causes it
Neurogenic bladder appears to stem from a host of underlying conditions, including:
• interstitial cystitis, cerebral disorders (such as stroke), brain tumor (such as meningioma and glioma), Parkinson’s disease, multiple sclerosis, dementia, and incontinence from aging
• spinal cord disease or trauma (such as spinal stenosis and arachnoiditis), cervical spondylosis, myelopathies from hereditary disorders or nutritional deficiencies and, rarely, tabes dorsalis
• disorders of peripheral innervation, including autonomic neuropathies resulting from endocrine disturbances such as diabetes mellitus (most common)
• metabolic disturbances such as hypothyroidism
• heavy metal toxicity
• chronic alcoholism
• collagen diseases such as lupus erythematosus
• vascular diseases such as atherosclerosis
• distant effects of cancer such as primary oat cell carcinoma of the lung
• herpes zoster.

Pathophysiology
An upper motor neuron lesion (at or above T12) causes spastic neurogenic bladder. A lower motor neuron lesion (at or below S2 to S4) affects the spinal reflex that controls voiding, with a resulting flaccid neurogenic bladder. Mixed neurogenic bladder results from an incomplete upper motor neuron, the result of cortical damage from some disorder or trauma.

What to look for
Neurogenic bladder produces a wide range of clinical effects depending on the underlying cause and its effect on the structural integrity of the bladder. All types of neurogenic bladder are associated with:
• some degree of incontinence
• changes in initiation or interruption of micturition
• an inability to empty the bladder completely. Vesicoureteral reflux, deterioration or infection in the upper urinary tract, and hydroureteral nephrosis may also result.

Spastic signs

Spastic neurogenic bladder signs and symptoms depend on the site and extent of the spinal cord lesion. They may include:
• involuntary, frequent, scant urination without a feeling of bladder fullness
• spontaneous spasms of the arms and legs
• increased anal sphincter tone
• voiding and spontaneous contractions of the arms and legs with tactile stimulation of the abdomen, thighs, or genitalia
• severe hypertension, bradycardia, and headaches, with bladder distention if cord lesions are in the upper thoracic (cervical) level.

Flaccid features

Clinical features of flaccid neurogenic bladder include:
• overflow incontinence
• diminished anal sphincter tone
• greatly distended bladder (evident on percussion or palpation) without the accompanying feeling of bladder fullness because of sensory impairment.

In the mix

Signs and symptoms of mixed neurogenic bladder include:
• dulled perception of bladder fullness and a diminished ability to empty the bladder
• urgency to void without control of the bladder.

What tests tell you
• Cerebrospinal fluid analysis showing increased protein levels may indicate cord tumor; increased gamma globulin levels may indicate multiple sclerosis.
• Skull and vertebral column X-rays may show fracture, dislocation, congenital anomalies, or metastasis.
• Myelography may show spinal cord compression.
• EEG may be abnormal if a brain tumor exists.
• Electromyelography can confirm peripheral neuropathy.
• Brain and CT scans can localize and identify brain masses.

Check the bladder

Tests specifically to assess bladder function include the following:
• Cystometry evaluates bladder nerve supply and detrusor muscle tone.
• A urethral pressure profile determines urethral function.
• Uroflowmetry shows diminished or impaired urine flow.
• Retrograde urethrography reveals strictures and diverticula.
• Voiding cystourethrography evaluates bladder neck function and continence.
• A postvoid residual determination test measures the amount of urine remaining in the bladder using a catheter or bladder ultrasonography.

How it’s treated
Bladder evacuation, drug therapy, surgery or, less commonly, neural blocks and electrical stimulation aim to maintain the integrity of the upper urinary tract, control infection, and prevent urinary incontinence.
Drug therapy may include oxybutynin, bethanechol, and phenoxybenzamine to promote bladder emptying and propantheline, flavoxate, dicyclomine, and imipramine (Tofranil) to facilitate urine storage. When drug therapy fails, the patient may require transurethral resection of the bladder neck, urethral dilation, external sphincterotomy, or a urinary diversion procedure to correct structural impairment. If permanent incontinence follows surgery, the patient may need an artificial urinary sphincter implanted.

What to do
• Watch for signs of infection (such as fever and cloudy or foulsmelling urine).
• Encourage the patient to drink plenty of fluids to prevent calculus formation and infection from urinary stasis. Try to keep the patient as mobile as possible.
• If the patient will undergo a urinary diversion procedure, arrange for consultation with an enterostomal therapist and coordinate the plans of care.
• Evaluate the patient. After successful therapy, the patient is free from infection, is continent, and verbalizes an understanding of his condition and the treatment techniques.

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Renal calculi

Renal calculi may form anywhere in the urinary tract but usually develop in the renal pelvis or calyces. Such formation follows precipitation of substances normally dissolved in the urine (calcium oxalate, calcium phosphate, magnesium ammonium phosphate or, occasionally, urate or cystine). Renal calculi vary in size and may be solitary or multiple. They may remain in the renal pelvis or enter the ureter and may damage renal parenchyma. Large calculi cause pressure necrosis. In certain locations, calculi cause obstruction (with resultant hydronephrosis) and tend to recur.

What causes it
Renal calculi may result from several causes:
• Decreased urine production from dehydration concentrates calculus-forming substances.
• An infection can result in damaged tissue that serves as a site for calculus development. Infected calculi (usually magnesium ammonium phosphate or staghorn calculi) may develop if bacteria serve as the nucleus in calculus formation. Such infections may promote destruction of renal parenchyma.
• Consistently acidic or alkaline urine provides a favorable medium for calculus formation.
• Urinary stasis (as in immobility from spinal cord injury) allows calculus constituents to collect and adhere, forming calculi. Obstruction also promotes infection which, in turn, compounds the obstruction.
• Increased intake of calcium or oxalate-rich foods encourage calculus formation.

• Immobility from spinal cord injury or other disorders allows calcium to be released into the circulation and, eventually, filtered by the kidneys.
• Metabolic factors — including hyperparathyroidism, renal tubular acidosis, elevated uric acid levels (usually with gout), defective metabolism of oxalate, genetically defective metabolism of cystine, and excessive intake of vitamin D, protein, or dietary calcium — may predispose a patient to renal calculi.

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Pathophysiology
Calculi form when substances normally dissolved in the urine, such as calcium oxalate and calcium phosphate, precipitate. Large, rough calculi may occlude the opening to the ureteropelvic junction. The frequency and force of peristaltic contractions increase, causing pain.

What to look for
Clinical effects vary with the size, location, and cause of the calculus. Pain is the key symptom. The pain of classic renal colic travels from the costovertebral angle to the flank, the suprapubic region, and the external genitalia. The pain fluctuates in intensity and may be excruciating at its peak. If calculi are in the renal pelvis and calyces, pain may be more constant and dull. Back pain occurs from calculi that produce an obstruction within a kidney. Nausea and vomiting usually accompany severe pain.
Other signs and symptoms include:
• abdominal distention
• fever and chills
• hematuria, pyuria and, rarely, anuria.

What tests tell you
• KUB X-rays reveal most renal calculi.
• Calculus analysis shows mineral content.
• Excretory urography confirms the diagnosis and determines the size and location of calculi.
• Renal ultrasonography may detect obstructive changes such as hydronephrosis.
• Urine culture of a midstream specimen may indicate UTI.
• Urinalysis results may be normal or may show increased specific gravity and acid or alkaline pH suitable for different types of calculus formation. Other urinalysis findings include hematuria (gross or microscopic), crystals (urate, calcium, or cystine), casts, and pyuria with or without bacteria and WBCs. A 24-hour urine collection is evaluated for calcium oxalate, phosphorus, and uric acid excretion levels.
• Other laboratory results support the diagnosis. Serial blood calcium and phosphorus levels detect hyperparathyroidism and show increased calcium levels in proportion to normal serum protein levels. Blood protein levels determine free calcium unbound to protein. Blood chloride and bicarbonate levels may show renal tubular acidosis. Increased blood uric acid levels may indicate gout as the cause.

How it’s treated
Because 90% of renal calculi are smaller than 5 mm in diameter, treatment usually consists of measures to promote their natural passage. Along with vigorous hydration, such treatment includes antimicrobial therapy (varying with the cultured organism) for infection; analgesics, such as meperidine and ketorolac tromethamine, for pain; and diuretics to prevent urinary stasis and further calculus formation (thiazide diuretics decrease calcium excretion into the urine, which reduces calculus formation).

Prophylaxis to prevent calculus formation includes a lowcalcium diet for absorptive hypercalciuria, parathyroidectomy for hyperparathyroidism, allopurinol for uric acid calculi, and daily administration of ascorbic acid by mouth to acidify the urine. A calculus that’s too large for natural passage may require surgical removal, percutaneous ultrasonic lithotripsy and ESWL, or chemolysis.

What to do
• Strain all urine through gauze or a urine strainer and save the solid material recovered for analysis.
• Promote sufficient intake of fluids to maintain a urine output of 3 to 4 L/day (urine should be very dilute and colorless). If the patient can’t drink the required amount of fluid, he can receive supplemental I.V. fluids. Record intake and output and daily weight to assess fluid status and renal function.
• If the patient requires surgery, reassure him by supplementing and reinforcing what the surgeon has told him about the procedure. Explain preoperative and postoperative care.
• Evaluate the patient. A successfully treated and counseled patient is free from pain, has recovered the calculus, and exhibits no signs of complications. He’s prepared to follow dietary and medical regimens, if necessary. He verbalizes a good understanding of his illness and the diagnostic procedures.

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