________________is usually not initially destroyed.
a. urine testing reveals a low specific gravity.
b. the causative factor is malignant hypertension.
c. urine testing reveals a high sodium concentration.
d. reversal of the oliguria occurs with fluid replacement.
Rationale: In prerenal oliguria, the oliguria is caused by a decrease in circulating blood volume, and there is no damage yet to the renal tissue. It can potentially be reversed by correcting the precipitating factor, such as fluid replacement for hypovolemia. Prerenal oliguria is characterized by urine with a high specific gravity and a low sodium concentration, whereas oliguria of intrarenal failure is characterized by urine with a low specific gravity and a high sodium concentration. Malignant hypertension causes damage to renal tissue and intrarenal oliguria.
b. specific gravity fixed at 1.010.
c. urine sodium of 12 meq/l (12mmol/L).
d. osmolality of 1000 mOsm/kg (1000 mmol/kg).
Rationale: A urine specific gravity that is consistently 1.010 and a urine osmolality of about 300 mOsm/kg is the same specific gravity and osmolality as plasma and indicates that tubules are damaged and unable to concentrate urine. Hematuria is more common with postrenal damage, and tubular damage is associated with a high sodium concentration (>40 mEq/L).
a. ammonia synthesis.
b. excretion of sodium.
c. excretion of bicarbonate.
d. conservation of potassium.
Rationale: Metabolic acidosis occurs in ARF because the kidneys cannot excrete H+, resulting in an increased acid load. Sodium is lost in urine because the kidneys cannot conserve sodium, and impaired excretion of potassium results in hyperkalemia. Bicarbonate is normally generated and reabsorbed by the functioning kidney to maintain acid-base balance.
a. massive trauma.
b. bladder obstruction.
c. decompensated heart failure.
d. acute glomerulonephritis.
Rationale: The normal BUN/creatinine ratio of 10:1 is increased in renal failure caused by conditions in which there is markedly increased catabolism, or breakdown of tissue, such as in severe injury, infections, or GI bleeding. The BUN is quite high in this case compared with the mild elevation of serum creatinine.
a. a return to normal weight.
b. a urine output of 3700 ml/day.
c. decreasing BUN and creatinine levels.
d. decreasing sodium and potassium levels.
Rationale: The BUN and creatinine levels remain high during the oliguric and diuretic phases of ARF. The recovery phase begins when the glomerular filtration returns to a rate at which BUN and creatinine stabilize and then decrease. Urinary output of 3 to 5 L/day, decreasing sodium and potassium levels, and fluid weight loss are characteristic of the diuretic phase of ARF.
a. urine output is 300 ml/24 hr.
b. edema occurs in the feet, legs, and sacral area.
c. the cardiac monitor reveals a depressed T wave and a sagging ST segment.
d. the patient experiences increasing muscle weakness and abdominal cramping.
Rationale: Hyperkalemia is a potentially life-threatening complication of ARF in the oliguric phase. Muscle weakness and abdominal cramping are signs of the neuromuscular impairment that occurs with hyperkalemia, in addition to cardiac conduction abnormalities of peaked T wave, prolonged PR interval, prolonged QRS interval, and depressed ST segment. Urine output of 300 ml/day is expected during the oilguric phase, as is the development of peripheral edema.
The most common cause of death in acute renal failure is irreversible metabolic acidosis. (infection)
Serum potassium and urea are increased during catabolism of body protein.
During the oliguric phase of acute renal failure, daily fluid intake is limited to 1000 ml plus the prior day’s measurable fluid loss.
600ml plus previous days total output
One of the most important nursing measures in managing fluid balance in the patient in acute renal failure is taking accurate daily weights.
Dietary sodium and potassium during the oliguric phase of acute renal failure are managed according to the patient’s urinary output.
(sodium and potassium serum levels)
b. Bicarbonate level of 14 mEq/L, indicating metabolic acidosis
c. Change in mental status
b. potassium level.
c. bicarbonate level.
d. the carbon dioxide level.
Rationale: During acidosis, potassium moves out of the cell in exchange for H+ ions, increasing the serum potassium level. Correction of the acidosis with sodium bicarbonate will help lower the potassium levels. A decrease in pH and the bicarbonate and PaCO2 levels would indicate worsening acidosis.
a. the total daily urine output.
b. the GFR.
c. serum creatinine and urea levels.
d. the degree of altered mental status.
Rationale: Stages of chronic kidney disease are based on the GFR or the presence of kidney damage over a period of 3 months. No specific markers of urinary output, azotemia, or urine output classify the degree of chronic kidney disease.
a. loss of aluminum through the impaired kidneys.
b. deposition of calcium phosphate in soft tissues if the body.
c. impaired vitamin D activation resulting in decreased GI absorption of calcium.
d. increased release of parathyroid hormone in response to decreased calcium levels.
Rationale: The calcium-phosphorus imbalances that occur in chronic kidney disease result in osteomalacia, osteitis fibrosa, and metatastic deposits of calcium phosphate, but pathologic fractures are most likely to occur from the osteomalacia resulting from hypocalcemia, which occurs from a deficiency of active vitamin D. Aluminum accumulation is also believed to contribute to the osteomalacia. Osteitis fibrosa involves replacement of calcium in the bone with fibrous tissue and is primarily a result of elevated levels of parathyroid hormone resulting from hypocalcemia.
a. a protein restriction of 70 g/day.
b. a potassium restriction of 2 to 3 g/day.
c. a sodium restriction of 1000 mg/day.
d. unlimited intake of breads and cereals.
Rationale: Conservative management of the patient with renal insufficiency with an elevated potassium level would include a dietary potassium restriction of 2 to 3 g (51 – 76 mEq), a protein restriction of 0.6 to 0.8 g/kg (42 – 56 g for this patient), and moderate (2 – 3 g) restriction of sodium unless there is marked edema or hypertension. Breads and cereals are not allowed in unrestricted amounts because they contain protein.
b. ice cream.
c. dill pickles.
d. hard candy.
Rationale: A patient with chronic kidney disease may have unlimited intake of sugars and starches (unless the patient is diabetic), and hard candy is an appropriate snack/treat and may help relieve the metallic and urine taste common in the mouth. Raisins are a high-potassium food, pickled foods have high sodium content, and ice cream contains protein.