What is the priority intervention for a patient with acute liver failure?

Choice A reason: Chloride levels are less critical in cirrhosis compared to sodium. Chloride imbalances may occur secondary to diuretic use or acid-base disturbances, but they do not directly drive major complications like ascites or edema. Monitoring is less urgent, as chloride fluctuations are typically managed indirectly through fluid and electrolyte balance.

Choice B reason: Calcium levels are not the primary concern in cirrhosis. Hypocalcemia may occur due to malnutrition or vitamin D deficiency from liver dysfunction, but it is less immediate than sodium imbalances. Calcium affects bone health and muscle function but does not directly impact acute cirrhosis complications like ascites.

Choice C reason: Sodium is critical to monitor in cirrhosis due to its role in fluid balance. Hyponatremia, common in advanced cirrhosis, results from impaired water excretion and portal hypertension, contributing to ascites and edema. Dilutional hyponatremia can worsen encephalopathy or indicate decompensation, requiring urgent management to stabilize the patient.

Choice D reason: Potassium monitoring is important, especially with diuretic use in cirrhosis, as hypokalemia or hyperkalemia can occur. However, sodium imbalances more directly influence fluid retention and ascites, making it a higher priority. Potassium affects cardiac and muscle function but is secondary to sodium in acute cirrhosis management.

Choice A reason: Metformin reduces blood sugar primarily by inhibiting hepatic gluconeogenesis, decreasing liver glucose production. It also enhances insulin sensitivity in peripheral tissues, reducing hyperglycemia in type 2 diabetes without causing hypoglycemia, as it does not stimulate insulin secretion, making this the accurate mechanism.

Choice B reason: Metformin does not block carbohydrate absorption in the intestine. Drugs like alpha-glucosidase inhibitors (e.g., acarbose) slow carbohydrate breakdown, but metformin primarily acts on the liver to reduce gluconeogenesis and improve insulin sensitivity, not directly affecting intestinal absorption.

Choice C reason: Metformin does not stimulate insulin release from the pancreas. This is the mechanism of sulfonylureas, which enhance beta-cell insulin secretion. Metformin works by reducing hepatic glucose output and increasing insulin sensitivity, making this statement incorrect for its mechanism of action.

Choice D reason: Metformin decreases, not increases, insulin resistance. It enhances insulin sensitivity in muscle and liver cells, improving glucose uptake and utilization. Increasing insulin resistance would worsen type 2 diabetes, making this statement incorrect, as metformin’s goal is to counteract insulin resistance.