Why does hypoglycemia occur in the majority of patients with fulminant hepatic failure?

Why does hypoglycemia occur in the majority of patients with fulminant hepatic failure?

• A. Impaired glycogenolysis, glycogenesis, gluconeogenesis and hyperinsulinemia
• B. Increased glycogen storage
• C. Enhanced gluconeogenesis
• D. Decreased insulin production

Answer: (A)

Massive liver failure disrupts the liver’s ability to regulate blood glucose. The liver normally maintains glucose during fasting by breaking down glycogen (glycogenolysis) and making new glucose (gluconeogenesis), and it also clears insulin from the bloodstream. When hepatocytes are injured, glycogenolysis and gluconeogenesis are severely impaired, so the liver can’t produce enough glucose. At the same time, the damaged liver cannot clear insulin effectively, leading to higher circulating insulin (hyperinsulinemia), which drives glucose into cells and lowers blood sugar further. This combination—reduced glucose production and increased insulin action—explains why hypoglycemia is common in fulminant hepatic failure. The other ideas don’t fit as well: increasing glycogen storage would tend to raise or stabilize glucose, enhancing gluconeogenesis would raise glucose levels, and decreased insulin production would make hypoglycemia less likely rather than more.

Massive liver failure disrupts the liver’s ability to regulate blood glucose. The liver normally maintains glucose during fasting by breaking down glycogen (glycogenolysis) and making new glucose (gluconeogenesis), and it also clears insulin from the bloodstream. When hepatocytes are injured, glycogenolysis and gluconeogenesis are severely impaired, so the liver can’t produce enough glucose. At the same time, the damaged liver cannot clear insulin effectively, leading to higher circulating insulin (hyperinsulinemia), which drives glucose into cells and lowers blood sugar further. This combination—reduced glucose production and increased insulin action—explains why hypoglycemia is common in fulminant hepatic failure.

The other ideas don’t fit as well: increasing glycogen storage would tend to raise or stabilize glucose, enhancing gluconeogenesis would raise glucose levels, and decreased insulin production would make hypoglycemia less likely rather than more.