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Biochemistry · Clinical biochemistry: hyperglycaemic emergencies
Sample itemA 74-year-old man with type 2 diabetes is drowsy and dehydrated after a week of infection. Plasma glucose is 900 mg/dL, effective osmolality 340 mOsm/kg, pH 7.36 and bicarbonate 22 mmol/L, with trace ketones. Why is ketosis minimal despite severe hyperglycaemia?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
D. Residual insulin is enough to restrain lipolysis and ketogenesis but not hepatic glucose output
Hyperosmolar hyperglycaemic state occurs when insulin is deficient or ineffective but still present in an amount that suppresses adipose lipolysis and hepatic ketogenesis. It is not enough to restrain gluconeogenesis and glycogenolysis, so glucose rises extremely, causing osmotic diuresis and dehydration. In diabetic ketoacidosis insulin is almost absent.
Option by option
A. A defect in hepatic carnitine palmitoyltransferase I
CPT-I failure would impair ketogenesis, but it is not a feature of this condition.
B. Rapid ketone use by the brain lowers blood levels
The brain cannot remove enough ketone bodies to hide ketosis, and ketone use would not prevent the formation seen in ketoacidosis.
C. Complete absence of insulin with very high glucagon
Absent insulin with high glucagon describes diabetic ketoacidosis, which has acidosis and heavy ketosis.
D. Residual insulin is enough to restrain lipolysis and ketogenesis but not hepatic glucose output (correct)
Correct. Low-level insulin action suppresses ketogenesis while hyperglycaemia continues.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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