Nursing Elites

1. What are the primary pathophysiological mechanisms responsible for ascites in liver failure?

• A. Decreased liver enzymes.
• B. Increased hydrostatic pressure in portal circulation.
• C. High bilirubin levels.
• D. Fluid shifts due to decreased serum proteins.

Correct answer: B

Rationale: The correct answer is B: Increased hydrostatic pressure in portal circulation. Ascites in liver failure is primarily caused by fluid shifts from the intravascular space to the interstitial space due to increased hydrostatic pressure in the portal circulation. Choice A is incorrect as ascites is not caused by decreased liver enzymes. Choice C is incorrect as high bilirubin levels are not the primary mechanism for ascites in liver failure. Choice D is incorrect as fluid shifts in ascites are due to decreased serum proteins, not increased serum proteins.

2. A client is experiencing acute bronchospasm. What is the nurse's priority intervention?

• A. Administer a nebulizer treatment of albuterol.
• B. Start an IV infusion of normal saline.
• C. Administer oxygen at 4L/min via nasal cannula.
• D. Position the client in a high Fowler's position.

Correct answer: A

Rationale: The correct answer is to administer a nebulizer treatment of albuterol. In acute bronchospasm, the priority intervention is to deliver a bronchodilator like albuterol to open the airways and improve breathing. Starting an IV infusion of normal saline (Choice B) may be necessary but not the priority in this situation. Administering oxygen at 4L/min via nasal cannula (Choice C) is important but not the first intervention for bronchospasm. Positioning the client in a high Fowler's position (Choice D) can help with breathing but is not the priority over administering a bronchodilator.

3. A client with a history of alcohol abuse presents with confusion and unsteady gait. The nurse suspects Wernicke's encephalopathy. Which treatment should the nurse anticipate?

• A. Thiamine supplementation
• B. Folic acid replacement
• C. Intravenous glucose
• D. Magnesium sulfate administration

Correct answer: A

Rationale: Wernicke's encephalopathy is a neurological condition commonly caused by a deficiency in thiamine, often seen in clients with chronic alcohol abuse. Thiamine supplementation is the primary treatment to prevent further neurological damage. Folic acid replacement (choice B) is not the correct treatment for Wernicke's encephalopathy. Intravenous glucose (choice C) may be necessary in some cases of Wernicke's encephalopathy, but thiamine supplementation takes precedence. Magnesium sulfate administration (choice D) is not indicated as the primary treatment for Wernicke's encephalopathy.

4. A client with heart failure receiving furosemide develops muscle weakness. What is the nurse's priority action?

• A. Administer potassium supplements as prescribed.
• B. Monitor the client’s potassium levels.
• C. Instruct the client to increase their salt intake.
• D. Discontinue the furosemide.

Correct answer: B

Rationale: Muscle weakness in a client receiving furosemide (a diuretic) is often a sign of hypokalemia, as furosemide increases potassium loss. Monitoring potassium levels is essential to identify and address any imbalances and prevent complications such as arrhythmias. Administering potassium supplements without monitoring the levels can lead to hyperkalemia, which has its own set of serious complications. Instructing the client to increase salt intake is not appropriate in this situation as it does not address the underlying electrolyte imbalance. Discontinuing furosemide abruptly can worsen heart failure symptoms; therefore, monitoring potassium levels and adjusting the treatment accordingly is the most appropriate action.

5. During the admission assessment of a 3-year-old with bacterial meningitis and hydrocephalus, which assessment finding is evidence of increased intracranial pressure (ICP)?

• A. Low blood pressure
• B. Increased respiratory rate
• C. Normal pupil reaction
• D. Sluggish and unequal pupillary responses

Correct answer: D

Rationale: Sluggish and unequal pupillary responses are indicative of increased intracranial pressure (ICP) in a child with bacterial meningitis and hydrocephalus. This finding suggests that the optic nerve is being compressed due to increased ICP, causing a delay in pupillary reactions. Such a delay is a critical sign of worsening ICP and necessitates immediate intervention. Low blood pressure and increased respiratory rate can occur in various conditions but are less specific to increased ICP than sluggish and unequal pupillary responses, which directly reflect neurological compromise.

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