A patient with a history of chronic obstructive pulmonary disease (COPD) and type 2 diabetes has been treated for pneumonia for the past week. The patient has been receiving intravenous corticosteroids as well as antibiotics as part of his therapy. At this time, the pneumonia has resolved, but when monitoring the blood glucose levels the nurse notices that the level is still elevated. What is the best explanation for this elevation?

Choice A rationale: Certain antibiotics, such as fluoroquinolones, can cause both hypo- and hyperglycemia, but this effect is less common and less pronounced than the effect of corticosteroids. The significant and sustained increase in blood glucose is more characteristic of steroid use, which is a known and common side effect. Choice B rationale: Corticosteroids stimulate gluconeogenesis in the liver and reduce glucose uptake in peripheral tissues, leading to insulin resistance. This combination results in a significant increase in blood glucose levels, a phenomenon known as steroid-induced hyperglycemia. The patient's type 2 diabetes exacerbates this effect. Choice C rationale: Type 2 diabetes does not convert to type 1 diabetes. These are distinct pathophysiological conditions. Type 1 is an autoimmune disease with absolute insulin deficiency, while type 2 involves insulin resistance and relative deficiency. The current elevated glucose is an acute, reversible effect of medication, not a change in the underlying disease. Choice D rationale: While hypoxia can lead to a stress response that increases blood glucose, it is not the primary cause of this sustained elevation in a patient on corticosteroids. The direct metabolic effects of corticosteroids on glucose metabolism are the most significant and likely cause of the observed hyperglycemia.