A nursing student asks a nurse to explain the differences between amphotericin B and the azoles group of antifungal agents. Which statement by the nurse is correct?

Choice A reason: Hyperbilirubinemia and jaundice are common manifestations of chronic liver disease, but they are not the primary cause of hepatic encephalopathy. These conditions result from the liver's inability to process and clear bilirubin effectively, leading to its accumulation in the blood and subsequent yellowing of the skin and eyes. While these symptoms indicate liver dysfunction, they do not directly cause the neurological impairments seen in hepatic encephalopathy.

Choice B reason: Fluid and electrolyte imbalances are often associated with chronic liver disease and can contribute to various complications, including ascites and edema. However, these imbalances are not the primary cause of hepatic encephalopathy. While electrolyte disturbances, particularly hyponatremia, can exacerbate encephalopathy, the condition itself is more directly linked to the liver's inability to detoxify certain substances, such as ammonia.

Choice C reason: Decreased cerebral blood flow can lead to neurological impairments, but it is not the primary mechanism underlying hepatic encephalopathy. Hepatic encephalopathy primarily results from the accumulation of neurotoxic substances that the liver can no longer effectively process, rather than reduced blood flow to the brain.

Choice D reason: Impaired ammonia metabolism and increased ammonia levels in the blood are the main causes of hepatic encephalopathy. In chronic liver disease, the liver's ability to convert ammonia, a byproduct of protein metabolism, into urea for excretion is compromised. As a result, ammonia accumulates in the blood and crosses the blood-brain barrier, leading to neurotoxicity and the characteristic symptoms of hepatic encephalopathy, such as confusion, altered consciousness, and asterixis (flapping tremor).

Choice A reason: Protein restriction is not a primary treatment for prerenal kidney injury. While managing protein intake can be important in chronic kidney disease to reduce the workload on the kidneys, it is not directly relevant to the acute management of prerenal kidney injury, which primarily involves restoring adequate blood flow to the kidneys.

Choice B reason: Potassium supplementation is not typically necessary for prerenal kidney injury. In fact, in many cases of kidney injury, there is a risk of hyperkalemia (elevated potassium levels) due to reduced kidney function. Therefore, potassium levels need to be monitored, but supplementation is not a standard treatment.

Choice C reason: Fluid administration to increase cardiac output is the appropriate therapy for prerenal kidney injury. Prerenal kidney injury is caused by reduced blood flow to the kidneys, often due to factors like hypovolemia (low blood volume) or heart failure. Administering fluids helps to restore adequate blood flow and perfusion to the kidneys, which can improve kidney function and resolve the prerenal injury.

Choice D reason: Fluid restriction is not appropriate for prerenal kidney injury, which is characterized by reduced blood flow to the kidneys. In cases where hypovolemia or low cardiac output is the cause, restricting fluids would worsen the condition. Instead, increasing fluid intake helps to restore adequate perfusion to the kidneys.