What is the main physiological reason for the elevated blood glucose in hyperglycemic hyperosmolar nonketotic state?

In hyperglycemic hyperosmolar nonketotic state (HHNS), the primary physiological driver behind elevated blood glucose levels is increased cortisol production. Cortisol is a glucocorticoid hormone released from the adrenal glands during stress and contributes significantly to glucose metabolism. It promotes gluconeogenesis, the process of generating glucose from non-carbohydrate sources, and inhibits the action of insulin, which leads to decreased glucose uptake by cells and results in sustained high blood glucose levels.

In the context of HHNS, patients often experience a severe lack of insulin or a significant resistance to insulin, leading to uncontrolled gluconeogenesis and hyperglycemia. While other factors such as dehydration and electrolyte imbalances also play a role, the elevation in cortisol production exacerbates hyperglycemia by promoting further glucose output from the liver and inhibiting cellular glucose uptake.

The other options do not accurately reflect the mechanisms at play in HHNS. Increased insulin sensitivity would actually help lower blood sugar levels, decreased glucagon secretion would not contribute to elevated glucose as glucagon raises blood sugar, and increased glucose uptake by cells would lead to lower blood glucose levels, not higher. Understanding the action of cortisol and its effects on glucose metabolism is crucial for grasping why elevated blood glucose occurs in