A 27-year-old man is brought to the emergency department due to confusion. His roommate says that he has been binge drinking for the last 5 days and probably has had very little to eat. The patient's medical history is significant for alcohol-related seizures 1 year ago. He had been sober until 2 weeks ago, when he started drinking again. The patient's past medical history is otherwise unremarkable. On examination, he responds to voice but does not follow commands. Fingerstick glucose is 35 mg/dL and urine is strongly positive for ketones. Suppression of which of the following is the primary cause of this patient's hypoglycemia?

Question

A 27-year-old man is brought to the emergency department due to confusion.  His roommate says that he has been binge drinking for the last 5 days and probably has had very little to eat.  The patient's medical history is significant for alcohol-related seizures 1 year ago.  He had been sober until 2 weeks ago, when he started drinking again.  The patient's past medical history is otherwise unremarkable.  On examination, he responds to voice but does not follow commands.  Fingerstick glucose is 35 mg/dL and urine is strongly positive for ketones.  Suppression of which of the following is the primary cause of this patient's hypoglycemia?

Quizplus · Accepted Answer

11ec160b_36a1_d747_9249_09c77c486ee8_MD0001_00 The metabolism of ethanol by alcohol dehydrogenase and aldehyde dehydrogenase reduces NAD⁺ to NADH and increases the NADH/NAD⁺ ratio. This inhibits all other pathways requiring NAD⁺, including reactions required for gluconeogenesis. In particular, lactate cannot be converted to pyruvate, and instead the reaction is driven from pyruvate toward lactate. In addition, excess NADH inhibits the conversion of malate to oxaloacetate. Pyruvate and oxaloacetate are intermediates in gluconeogenesis; therefore, conversion of these molecules to lactate and malate inhibits gluconeogenesis. Alcohol does not inhibit glycogenolysis (Choice B), and so in the initial phase of binge drinking (heavy alcohol intake with reduced nutritional carbohydrate intake), hepatic glycogenolysis is able to maintain euglycemia. However, after a prolonged binge, hepatic glycogen is eventually depleted and blood glucose levels drop. (Choices C and D) Ethanol has no direct effect on insulin sensitivity. Impaired clearance of insulin is a major contributor to hypoglycemia in patients with advanced renal insufficiency. (Choice E) Excess NADH inhibits free fatty acid oxidation, thereby diverting free fatty acids away from lipolysis to the formation of triglycerides. This contributes to alcohol-induced hepatic steatosis but does not cause hypoglycemia. Educational objective: Ethanol inhibits gluconeogenesis and can cause hypoglycemia once hepatic glycogen stores are depleted. __________ References: Case of alcoholic ketoacidosis accompanied with severe hypoglycemia. (http://www.ncbi.nlm.nih.gov/pubmed/25787101)

A 27-Year-Old Man Is Brought to the Emergency Department Due