The nurse is caring for a client with kidney failure. Which assessment data indicates the need for increased fluids?
Increased blood urea nitrogen (BUN)
Decreased sodium level
Increased creatinine level
Pale-colored urine
The Correct Answer is A
Blood urea nitrogen (BUN) is a metabolic byproduct of protein catabolism that is normally filtered by the glomeruli. While it is a marker of renal function, it is also highly sensitive to volume status. In cases of dehydration or pre-renal azotemia, the slower flow of filtrate through the tubules allows for increased reabsorption of urea into the blood, leading to an elevated BUN disproportionate to creatinine levels.
Rationale:
A. An increased blood urea nitrogen (BUN) often indicates a state of dehydration or pre-renal azotemia, suggesting the need for increased fluid intake. When intravascular volume is low, renal perfusion decreases, causing the BUN to rise. If the BUN-to-creatinine ratio exceeds 20:1, it strongly suggests that the patient's renal function is being hampered by insufficient fluid volume.
B. A decreased sodium level, or hyponatremia, in a kidney failure patient usually indicates fluid volume excess rather than a need for more fluids. This is typically a "dilutional" hyponatremia where the patient has retained too much water relative to sodium. Adding more fluids in this scenario would worsen the electrolyte imbalance and increase the risk of cerebral edema.
C. Increased creatinine levels signify intrinsic damage to the nephrons and a reduction in the glomerular filtration rate. Unlike BUN, creatinine is not significantly affected by hydration status alone and is a more permanent marker of kidney damage. Raising fluid intake may not necessarily lower creatinine if the underlying renal tissue is chronically scarred or acutely necrotic.
D. Pale-colored urine indicates that the urine is dilute and the kidneys are successfully excreting water. This is a sign of adequate hydration rather than a need for increased fluid intake. In kidney failure, the inability to concentrate urine can also result in pale urine, but it never serves as an indicator for more fluid administration.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Prothrombin time(PT) measures the integrity of the extrinsic and common pathways of the coagulation cascade. This diagnostic test evaluates the activity of clotting factors I, II, V, VII, and X. These essential clotting proteinsare synthesized exclusively in the liverusing Vitamin K. Consequently, a significant elevation in PT often serves as a sensitive biomarker for acute or chronic hepatic failure.
Rationale:
A.The liver is the primary site for the synthesis of most coagulation factors. When hepatic function is impaired due to cirrhosis or hepatitis, the production of these proteins decreases, leading to a prolonged prothrombin time. This makes PT a critical lab value for assessing the severity of hepatic dysfunctionand the patient's overall risk for spontaneous bleeding.
B.The spleen is primarily involved in the filtration of blood and the storage of platelets, not the synthesis of clotting factors. While an enlarged spleen (splenomegaly) can cause thrombocytopenia by sequestering platelets, it does not directly affect the prothrombin time. PT is a measure of plasma proteins, whereas the spleen’s hematologic role involves cellular components.
C.The kidneys play a major role in filtering waste and regulating erythropoietin, but they do not produce the clotting factors measured by the prothrombin time. Renal failure can lead to platelet dysfunction (uremia), but it does not cause the protein-based coagulation delays seen in liver disease. Therefore, prolonged PT is not a primary indicator of kidney damage.
D.The stomach is involved in the mechanical and chemical digestion of food and does not participate in the synthesis of coagulation proteins. While gastric issues can lead to bleeding, the cause would be structural (like an ulcer) rather than a systemic deficiency in clotting factors. Prolonged PT is a metabolic indicator of liver failure, not a gastric pathology.
Correct Answer is ["A","B","E","F"]
Explanation
Chronic pancreatitisis a progressive inflammatory disorder characterized by the irreversible destruction of pancreatic parenchyma and its replacement with fibrotic tissue. This results in both exocrine and endocrine insufficiency. The loss of acinar cells leads to malabsorption, while the destruction of Islets of Langerhansresults in secondary diabetes mellitus. Clinical manifestations reflect the body’s inability to digest fats and regulate systemic glucose homeostasis.
Rationale:
A.Polyuriais expected in chronic pancreatitis due to the destruction of beta cells in the pancreas, leading to secondary diabetes mellitus. When insulin production fails, blood glucose rises, exceeding the renal threshold for reabsorption. This leads to osmotic diuresis, where the excess glucose in the urine pulls water with it, increasing the frequency and volume of urination.
B.Jaundiceoccurs in chronic pancreatitis when fibrotic changes or inflammation in the head of the pancreas compress the common bile duct. This mechanical obstruction prevents the flow of bile into the duodenum, causing conjugated bilirubinto back up into the bloodstream. This manifests as yellowing of the skin and sclera, indicating impaired biliary drainage due to pancreatic structural damage.
C.Weight gain is not expected; instead, weight loss is a hallmark of chronic pancreatitis. The loss of exocrine enzymes means the body cannot break down and absorb nutrients effectively. Combined with the metabolic demands of chronic inflammation and the onset of diabetes, patients typically present with significant malnutritionand unintentional weight loss over time.
D.Ascites is primarily a complication of liver cirrhosis and portal hypertension, rather than chronic pancreatitis. While pancreatic ascites can occur in rare cases of ductal rupture, it is not a standard finding. The primary pathological process in chronic pancreatitis involves parenchymal fibrosisand enzyme deficiency rather than the systemic venous congestion that typically produces peritoneal fluid accumulation.
E.Steatorrhea, or fatty, foul-smelling stools, is a classic finding resulting from exocrine insufficiency. Without adequate lipase secretion, the body cannot emulsify and absorb dietary lipids. The undigested fat remains in the intestinal lumen, leading to stools that are voluminous, greasy, and difficult to flush. This signifies a total breakdown of the digestive functionof the pancreas.
F.Polydipsia, or excessive thirst, is a direct consequence of the hyperglycemia-induced polyuria associated with pancreatic endocrine failure. As the patient loses large volumes of fluid through the kidneys, the thirst center in the hypothalamus is stimulated to prevent dehydration. This is a key symptom of the secondary diabetesthat develops as the Islets of Langerhans are destroyed.
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