Patho Test 5 NCLEX Q's part 2 of 2 Renal

38. ________ is both a cause of chronic kidney disease and a result of chronic kidney disease.

ANS: Hypertension Hypertension is both a cause of chronic kidney disease and a result of chronic kidney disease.

37. The best intervention for acute kidney injury (AKI) is ________.

ANS: prevention The best intervention for acute kidney injury is prevention.

29. Individuals with end-stage chronic renal disease are at risk for renal osteodystrophy and spontaneous bone fractures, because a. excess potassium leaches calcium from bone. b. erythropoietin secretion is impaired. c. urea causes demineralization of bone. d. they are deficient in active vitamin D.

ANS: D Vitamin D, required for calcium absorption in the digestive tract, is activated in the kidneys. With chronic renal failure, vitamin D is not activated. Hyperkalemia does not influence bone mineralization. Erythropoietin is important for red blood cell production. Urea does not cause renal osteodystrophy.

15. One of the most common causes of acute tubular necrosis (ATN) is a. ischemic conditions. b. cytotoxic agents. c. immune reaction. d. prolonged postrenal kidney injury.

ANS: A Ischemia and nephrotoxic agents are the most common causes of ATN. Cytotoxic agents, immune reaction, and prolonged postrenal kidney injury are not the most common causes of ATN.

4. Appropriate therapy for prerenal kidney injury includes a. fluid administration. b. potassium supplementation. c. fluid restriction. d. protein restriction.

ANS: A Appropriate therapy for prerenal oliguria includes fluid administration; most often prerenal kidney injury is due to fluid volume deficit. Potassium supplements are not appropriate in prerenal oliguria, as potassium is not being excreted. Appropriate therapy for prerenal oliguria includes fluid administration. Protein restriction is not indicated in prerenal oliguria.

13. At his most recent clinic visit, a patient with end-stage renal disease is noted to have edema, congestive signs in the pulmonary system, and a pericardial friction rub. Appropriate therapy at this time would include a. initiation of dialysis. b. fluid restriction. c. antibiotics. d. phlebotomy.

ANS: A Dialysis is the appropriate therapy at end-stage renal disease. Although fluid restriction may be appropriate at some point in renal failure, it will not correct the identified problems. Antibiotics will not correct the problems identified and may further impair remaining renal function. Phlebotomy will not correct the identified problems.

20. One of the most frequent causes of chronic kidney disease is a. hypertension. b. glomerulonephritis. c. chronic pyelonephritis. d. polycystic kidney disease.

ANS: A Hypertension and diabetes are the most common causes of chronic kidney disease. Although glomerulonephritis, chronic pyelonephritis, and polycystic kidney disease can result in CKD, hypertension and diabetes are the most common causes of chronic kidney disease.

2. Osteoporosis commonly occurs in patients with end-stage renal disease because of a. hyperparathyroidism. b. hypercalcemia. c. excess active vitamin D. d. phosphorous deficiency.

ANS: A Osteoporosis commonly occurs in patients with end-stage renal disease because of hyperparathyroidism. Hypocalcemia occurs in end-stage renal disease. Insufficient active vitamin D would result in osteoporosis. Phosphate is retained in end-stage renal disease.

21. The patient most at risk for post-renal acute kidney injury is a(n) a. elderly patient with hypertrophy of the prostate. b. middle-aged woman with bladder infection. c. young child with reflux at the ureterovesical junction. d. patient who has both hypertension and diabetes.

ANS: A Post-renal acute kidney injury is caused by obstruction in the urinary tract below the level of the kidneys. Elderly men with prostatic hypertrophy are at risk for urinary retention. Bladder infection generally does not obstruct urine flow. Ureterovesical junction reflux is likely to cause pyelonephritis, but not obstruction. Diabetes and hypertension result in intra-renal disease.

27. Prerenal acute kidney injury may be caused by a. severe hypotension. b. glomerulonephritis. c. bilateral kidney stones. d. acute tubular necrosis.

ANS: A Prerenal acute kidney injury occurs when blood flow to the kidneys is compromised. Severe hypotension from heart failure, hypovolemia, or shock is a leading cause. Glomerulonephritis does not cause prerenal acute kidney injury, because the glomeruli are located within the kidneys. Bilateral kidney stones do not cause prerenal acute kidney injury, because they are located distal to the nephrons. Acute tubular necrosis does not cause prerenal acute kidney injury, because the renal tubules are located within the kidneys.

8. The most helpful laboratory value in monitoring the progression of declining renal function is a. serum creatinine. b. serum potassium. c. blood urea nitrogen. d. mental status changes.

ANS: A Serum creatinine is the most stable and accurate reflection of renal function. Serum potassium is affected by many factors and thus not the most helpful value in monitoring the progression of this disease. Blood urea nitrogen is not as stable as serum creatinine; it is affected by muscle breakdown, protein intake, and so forth. Mental status changes can occur due to multiple factors other than renal function.

17. The most common agent resulting in nephrotoxicity and subsequent acute tubular necrosis (ATN) in hospitalized patients is a. contrast media. b. antibiotics. c. cancer chemotherapy. d. recreational drugs.

ANS: A The most common agent resulting in nephrotoxicity and subsequent ATN is contrast media. Contrast media, cancer chemotherapy, and recreational drugs are not the most common agents resulting in nephrotoxicity and subsequent ATN.

6. The most likely cause of anemia in a patient with end-stage renal disease is a. insufficient erythropoietin. b. blood loss secondary to hematuria. c. vitamin B12 deficiency secondary to deficient intrinsic factor. d. iron deficiency.

ANS: A The most likely cause of anemia in a patient with end-stage renal disease is insufficient erythropoietin secretion by the kidney, which is necessary for RBC production. Blood loss secondary to hematuria, vitamin B12 deficiency secondary to deficient intrinsic factor, and iron deficiency are not the most likely causes of anemia in a patient with end-stage renal disease.

1. The oliguric phase of acute tubular necrosis is characterized by a. fluid excess and electrolyte imbalance. b. fever and diminishing cognition. c. sodium retention and potassium loss in the urine. d. magnesium and phosphorous loss in the urine.

ANS: A The oliguric phase of ATN is characterized by fluid excess and electrolyte imbalance. Fever and diminishing cognition are not typical manifestations of ATN oliguric phase. During this phase sodium is lost in the urine and potassium is not excreted, and magnesium and phosphorous are retained in the body.

18. The risk for contrast media-induced acute tubular necrosis (ATN) is highest in a. a 70-year-old patient with heart failure. b. a 50-year-old patient post gallbladder surgery. c. a 12-year-old patient with recurrent bladder infections. d. a 30-year-old patient with appendicitis.

ANS: A This patient with the highest risk has two risk factors for contrast media-induced ATN: age over 70 and co-existing heart failure. The other patients have no risk factors for contrast media-induced ATN.

36. When a patient misses two dialysis sessions numerous electrolyte imbalances resulted. The patient will likely demonstrate (Select all that apply.) a. lethargy due to metabolic acidosis and increased BUN. b. skeletal muscle weakness and possible cardiac dysrhythmias due to hyperkalemia. c. positive Chvostek and Trousseau signs due to hypomagnesemia. d. weight gain of several pounds since her last dialysis session due to hypernatremia. e. deep rapid breathing due to compensatory mechanism for metabolic acidosis.

ANS: A, B, E A person who needs dialysis and has missed two sessions will have metabolic acidosis and increased BUN, which cause lethargy; deep rapid breathing, which is a compensatory mechanism for metabolic acidosis; and hyperkalemia, which causes skeletal muscle weakness and cardiac dysrhythmias. Hypomagnesemia will not occur in this situation. Although the individual will gain several pounds of fluid without dialysis, the weight gain is due to extracellular fluid volume excess rather than to hypernatremia.

33. Signs of late chronic renal failure include (Select all that apply.) a. high-serum potassium levels. b. high-serum calcium. c. high-serum phosphorous. d. high-blood urea nitrogen. e. anemia.

ANS: A, C, D, E In late chronic renal failure high serum potassium and phosphorous levels are due to inability of the kidneys to excrete these elements. Blood urea also increases due to inability of the kidneys to excrete urea. Anemia occurs due to loss of erythropoietin secretion. The serum calcium is low in chronic renal failure because of the high serum phosphorous.

34. The diet for a patient with chronic kidney disease (CKD) should include (Select all that apply.) a. high carbohydrates and fats. b. low sodium and potassium. c. high protein. d. low phosphorous. e. high calorie.

ANS: A, D, E Patients with CKD are often malnourished especially at later stages. Patients require high carbohydrates and fats to maintain nutritional status. Sodium must be limited due to fluid retention and potassium must be limited due to failure of kidneys to excrete potassium. Low phosphorous is necessary to prevent further hypocalcemia. High calories are needed to maintain energy needs. In general protein must be limited, as the kidneys cannot excrete urea, the end product of protein metabolism.

22. The defining characteristic of severe acute kidney injury is a. proteinuria. b. oliguria. c. hematuria. d. diuresis.

ANS: B Acute kidney injury is defined by oliguria or anuria. Proteinuria, hematuria, and diuresis are not defining characteristics of severe acute kidney injury.

3. Gastrointestinal drainage, perioperative and postoperative hypotension, and hemorrhage may all contribute to renal failure by causing a. hydronephrosis. b. acute tubular necrosis. c. nephrosis. d. renal inflammation.

ANS: B Gastrointestinal drainage, perioperative and postoperative hypotension, and hemorrhage may all contribute to renal failure by causing acute tubular necrosis. Gastrointestinal drainage, perioperative and postoperative hypotension, and hemorrhage do not cause hydronephrosis, nephrosis, or renal inflammation.

32. A patient injured severely in a motor vehicle accident is hospitalized with acute kidney injury as well as multiple broken bones and lacerations. When family members ask what is meant by the term 'prerenal,' the nurse responds a. "The doctors are not sure what caused your husband's acute kidney injury, but they are working to help him recover." b. "Your husband's kidney injury did not start in the kidney itself, but rather in the blood flow to the kidney." c. "Your husband's kidney injury is only the beginning of the problems that are expected, so they are being vigilant." d. "Acute kidney injury is a new term for what people used to call acute renal failure."

ANS: B The problem that triggers prerenal acute kidney injury occurs before the blood circulates to the kidney. Hypovolemia is a common cause of prerenal acute kidney injury. Providing the patient's family with specific information is most effective. Telling the family that you don't know what caused the injury does not alleviate anxiety in the family member. Speculating about the patient's future without a clear prognosis causes anxiety in the patient. It is best to provide the family with specific information regarding the patient's diagnosis and prognosis instead of offering general comments.

14. The most common cause of intrinsic kidney injury is _____ injury. a. glomerular b. tubular c. interstitial d. vascular

ANS: B Tubular injury (acute tubular necrosis) is the most common cause of acute kidney injury. Glomerular, interstitial, and vascular injury are not the most common causes of acute kidney injury.

35. Acute tubular necrosis can occur from (Select all that apply.) a. increased ammonia levels from liver failure. b. contrast dyes used for radiologic studies. c. ischemia due to hypovolemia. d. antibiotics that are nephrotoxic.

ANS: B, C, D Radiocontrast media used for radiologic studies occasionally can be nephrotoxic, causing acute tubular necrosis. Ischemia due to hypovolemia is an important cause of acute tubular necrosis. Certain antibiotics, including aminoglycosides, are nephrotoxic and can be a direct cause of acute tubular necrosis. Liver failure with elevated ammonia levels causes toxicity to the central nervous system but does not cause acute tubular necrosis.

28. Postrenal acute kidney injury may be caused by a. severe hypotension. b. glomerulonephritis. c. bilateral kidney stones. d. acute tubular necrosis.

ANS: C Bilateral kidney stones can cause postrenal acute kidney injury due to obstruction of normal outflow of urine from the kidneys. Severe hypotension causes prerenal acute kidney injury. Glomerulonephritis does not cause postrenal acute kidney injury, because the glomeruli are located within the kidneys. Acute tubular necrosis does not cause postrenal acute kidney injury, because the renal tubules are located within the kidneys.

30. Anemia in people who have end-stage chronic renal disease is caused by a. chronic loss of blood in the urine. b. poor appetite, with lack of iron intake. c. decreased secretion of erythropoietin. d. increased secretion of aldosterone.

ANS: C Decreased secretion of erythropoietin is the major cause of anemia in end-stage chronic renal disease. Hematuria is not a characteristic of end-stage chronic renal disease. Iron deficiency does not cause the anemia in end-stage chronic renal disease. Aldosterone levels do not contribute to anemia.

9. Appropriate management of end-stage renal disease includes a. potassium supplementation. b. a high-protein diet. c. erythropoietin administration. d. a high-phosphate diet.

ANS: C Erythropoietin administration is appropriate, as the kidneys are not able to secrete erythropoietin. Potassium is not appropriate, as the kidneys are unable to excrete potassium. A high-protein diet is not appropriate, as the kidneys are unable to excrete urea. A high-phosphate diet is not appropriate, as the kidneys are unable to excrete phosphorous.

25. Renal insufficiency occurs when _____ of the nephrons are not functional. a. 25% b. 50% c. 75% to 90% d. more than 90%

ANS: C In renal insufficiency, 75% to 90% of the nephrons are not functional. When 25% to 50% of nephrons are not functional, it is decreased renal reserve. When 90% of nephrons are not functional, it is end-stage renal disease.

7. The most likely cause of acidosis in a patient with end-stage renal disease is a. insufficient filtration of bicarbonate ions at the glomerulus. b. excessive production of respiratory and metabolic acids. c. insufficient metabolic acid excretion due to nephron loss. d. hypoventilation secondary to uremic central nervous system depression.

ANS: C The most likely cause of acidosis in a patient with end-stage renal disease is insufficient metabolic acid excretion due to nephron loss. Insufficient filtration of bicarbonate at the glomerulus would lead to alkalosis, not acidosis. Excessive production of respiratory acids would lead to respiratory acidosis not metabolic acidosis. The problem is metabolic acids are not excreted. Hypoventilation secondary to uremic CNS depression may occur, but this would lead to respiratory acidosis, not metabolic acidosis.

10. What problem is a patient likely to experience in end-stage renal disease? a. Hypokalemia b. Polyuria and nocturia c. Uremia d. Hematuria

ANS: C Uremia occurs in end-stage renal disease because the kidneys cannot excrete urea, the end product of protein metabolism. Hyperkalemia occurs in end-stage renal disease. Polyuria and nocturia do not occur in end-stage renal disease; the kidneys are unable to excrete urine. Hematuria does not generally occur unless another problem is causing it.

5. A patient with renal disease is at risk for developing uremia as the nephrons progressively deteriorate, because a. the basement membrane becomes increasingly permeable. b. filtration exceeds secretory and reabsorptive capacity. c. excessive solute and water are lost in the urine. d. GFR declines.

ANS: D A patient with renal disease is at risk for developing uremia as his nephrons progressively deteriorate because GFR declines. The basement membrane does not become increasingly permeable. Filtration does not exceed secretory and reabsorptive capacity. Excessive solute and water are not lost in the urine.

11. Which intervention has been found to retard the advancement of chronic kidney disease? a. Calcium supplementation b. Erythropoietin c. Insulin d. ACE inhibitors

ANS: D ACE inhibitors or A-II receptor blockers have been found to retard the advancement of chronic kidney disease by reducing proteinuria. Calcium supplementation, erythropoietin, and insulin have not been found to retard the advancement of chronic kidney disease.

26. The effect on the renal tubules during the postoliguric phase of acute tubular necrosis involves a. reconstruction of the basement membrane. b. blocking the tubule lumens by dead cells. c. making the glomeruli patent again. d. regeneration of the renal tubular epithelium.

ANS: D During the postoliguric phase of acute tubular necrosis, the renal tubular epithelium is regenerating. Disruption of basement membranes is not characteristic of acute tubular necrosis. Blockage of the tubule lumens would cause oliguria. The glomeruli are not clogged during acute tubular necrosis.

23. A primary laboratory finding in end-stage chronic renal disease is a. decreased blood urea nitrogen (BUN). b. decreased serum sodium. c. metabolic alkalosis. d. increased serum creatinine.

ANS: D End-stage chronic renal disease causes increased serum creatinine and blood urea nitrogen, because the dysfunctional kidneys are not able to excrete these metabolic waste products. Chronic renal failure causes increased blood urea nitrogen. Hyponatremia is not a primary laboratory finding in end-stage chronic renal disease. Metabolic alkalosis is not common with end-stage chronic renal disease.

12. In patients with polycystic kidney disease, renal failure is expected to progress over time as the cystic process destroys more nephrons. At what point will a patient reach end-stage renal disease? a. Greater than 15% b. Greater than 25% nephron loss c. Greater than 50% nephron loss d. Greater than 90% nephron loss

ANS: D End-stage renal disease occurs when greater than 90% of the nephrons have been lost. End-stage renal disease is possible to predict based on nephron loss. It occurs when greater than 90% (not 15%, 25% or 50%) of the nephrons have been lost.

24. The condition associated with end-stage chronic renal disease that is the most immediately life threatening is a. azotemia. b. increased creatinine. c. hypertension. d. hyperkalemia.

ANS: D Hyperkalemia from decreased renal excretion of potassium can cause dysrhythmias and cardiac arrest. While azotemia, increased creatinine, and hypertension are consequences of end-stage chronic renal disease, they usually are not acutely life threatening.

19. If acute tubular necrosis (ATN) does not resolve and continued tubular dysfunction ensues, the patient will then experience a. oliguria and sodium retention. b. infections and sepsis. c. magnesium and phosphorus loss in urine. d. polyuria and sodium wasting.

ANS: D If ATN does not resolve, the high blood urea nitrogen (BUN) creates osmotic diuresis; the urine is high in sodium content. Oliguria and sodium retention, infections and sepsis, and magnesium and phosphorous loss in the urine do not result from tubular necrosis and tubular dysfunction.

16. The most common cause of ischemic acute tubular necrosis (ATN) in the United States is a. hypotension. b. hypovolemia. c. renal artery stenosis. d. sepsis.

ANS: D Sepsis is the most common cause of ischemic ATN in the United States. Hypotension, hypovolemia, and renal artery stenosis are not the most common causes of ischemic ATN.