ATI Fluid Electrolyte and Acid-Base Regulation

Correct Answer: D

Rationale: The correct answer is D. The man's elevated heart rate, anxiety, and low urine output indicate a sympathetic reaction. This reaction stimulates the renin-angiotensin-aldosterone system, leading to decreased urine output. The sympathetic response triggers the release of renin, which activates angiotensin II and aldosterone, causing vasoconstriction and water reabsorption in the kidneys, ultimately reducing urine output. Choice A is incorrect because low urine output is not solely due to urinating before arrival. Choice B is incorrect as there is no indication of traumatic brain injury or ADH deficiency. Choice C is incorrect as atrial natriuretic peptide in heart failure typically increases urine output.

Correct Answer: B

Rationale: The correct answer is B: Malnourished patients receiving parenteral nutrition are at risk for hypophosphatemia if calories are started too aggressively. Patient with pancreatitis may have depleted levels of phosphorus due to malnutrition, and rapid initiation of TPN can further decrease phosphorus levels, leading to hypophosphatemia. This can result in respiratory failure, muscle weakness, and arrhythmias. Choice A is incorrect because patients receiving TPN are not specifically at risk for hypercalcemia due to rapid initiation of calories. Choice C is incorrect because rapid fluid infusion can lead to hypernatremia, not related to TPN initiation. Choice D is incorrect because the rationale provided for slow initiation is not related to digestive enzymes but rather to prevent hypophosphatemia in malnourished patients.

Correct Answer: A

Rationale: The correct answer is A: Substantially reduced renal function. In older adults, elevated serum creatinine levels can indicate impaired kidney function, as the kidneys may not filter waste products as efficiently. This can lead to a buildup of creatinine in the blood. Acute kidney injury (Choice B) is a sudden decline in kidney function and would typically present with a more significant increase in creatinine levels. Decreased cardiac output (Choice C) would not directly cause elevated creatinine levels. Alterations in the ratio of body fluids to muscle mass (Choice D) would not be a common cause of elevated creatinine levels in this scenario.

Correct Answer: A

Rationale: The correct answer is A because electrolyte-free water, such as sterile water, can rapidly enter red blood cells due to osmotic differences, causing them to swell and potentially rupture, leading to hemolysis. This can result in severe harm to the patient. Choice B is incorrect because electrolyte-free water is not indicated for severely dehydrated patients with neurologic signs and symptoms. They require electrolytes to correct their imbalances. Choice C is incorrect as administering electrolyte-free water would not address excess calcium and/or magnesium ions in the body. Specific treatments for hypercalcemia or hypermagnesemia are needed. Choice D is incorrect because patients with fluid deficits due to renal failure require electrolyte-balanced solutions to manage their condition effectively. Electrolyte-free water would not address the electrolyte imbalances associated with renal failure.

Correct Answer: B

Rationale: Correct Answer: B - The kidneys excrete hydrogen ions and conserve bicarbonate ions to help restore balance. Rationale: 1. In metabolic acidosis, the blood pH is low due to excess acid in the body. 2. To restore pH balance, the kidneys excrete hydrogen ions (acid) and conserve bicarbonate ions (a base). 3. By excreting acid and retaining base, the kidneys help neutralize the excess acid in the body. 4. Option B accurately describes the role of the kidneys in metabolic acidosis. Incorrect Choices: A: Incorrect. The kidneys do not retain hydrogen ions in metabolic acidosis; they excrete them. C: Incorrect. While the kidneys do play a role in correcting imbalances, they do not react rapidly in metabolic acidosis. D: Incorrect. The kidneys do regulate bicarbonate levels, but this is not the primary action in metabolic acidosis.